Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ten patients with severe hematologic malignancies (four with acute leukemia, three with multiple myeloma, one with prolymphocytic leukemia, one with malignant lymphoma and one with blastic crisis of chronic myelogenous leukemia) developed respiratory failure during the period between April 1986 and May 1990. Clinically, the patients manifested high-fever, dyspnea refractory to oxygen therapy, diffuse pulmonary rales and severe hypoxemia without evidence of cardiogenic pulmonary edema. Chest roentgenograms displayed diffuse alveolar infiltrates. Respiratory failure occurred as early as 48 hours and as late as 66 days after the administration of intensive anti-neoplastic chemotherapy. At that time leukocyte count was between 100/microliters and 54,900/microliters. Marked leukocytosis was observed in two patients with AML and PLL. Respiratory failure was preceded by sepsis in one patient with AML and by pneumonia in nine patients. DIC was diagnosed in four patients. All patients treated with high dose methyl prednisolone (mPSL) within 12 hours after the onset of respiratory failure. Only one patient required assisted ventilation. High dose mPSL had significant effect on seven of ten patients. But three patients died from progressive respiratory failure, sepsis, pneumonia and multi-organ failure.
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PMID:[Clinical investigation on acute respiratory failure in patients with severe hematologic malignancy]. 194 22

Hybridoma cells were obtained by fusing spleen cells from mice, immunized against the 15 kDa porcine surfactant apoprotein, with a myeloma cell line. Adult mice were inoculated intraperitoneally with this hybridoma; mice that were not inoculated or were inoculated with myeloma cells served as controls. Lung-thorax compliance was measured at various intervals after inoculation. The animals were then killed for histologic-morphometric evaluation of alveolar air expansion, inflammatory reaction in the pulmonary parenchyma, and intraalveolar edema. In the hybridoma group, the mice developed respiratory failure 9 days after inoculation, with markedly reduced lung-thorax compliance, lung congestion, alveolar collapse, hemorrhagic pulmonary edema, and hyaline membranes. Morphometric data from the same animals showed reduced volume density of alveolar air, and increased volume densities of intraalveolar "fluid" (edema) and tissue components. These lung lesions are similar to those in the adult respiratory distress syndrome.
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PMID:Respiratory failure in mice caused by a hybridoma making antibodies to the 15 kDa surfactant apoprotein. 339 79

From January 1980 to September 1985, 82 patients with IA to IIIB clinical stage (CS) Hodgkin's disease were treated by three MOPP chemotherapy (CT) cycles followed by extended field radiotherapy (RT) including the spleen (30-40 Gy). 2 patients died during the treatment (medullary aplasia, pulmonary edema). 6 were in failure after three MOPP cycles; they received other CT; 3 died and 3 are alive in remission (survival: 2.5 to 3.5 yr). 74 were in complete remission (CR) after completion of treatment. 4 patients relapsed (all alive after re-treatment) and 4 died in first CR (tuberculosis, hepatitis, myeloma, unknown cause). At 6 yr, actuarial survival and relapse-free survival are respectively 89.8% for the 82 patients and 93% for those in CR. These good results are due to: the administration of CT before RT, limited to three cycles; identification of failures after CT; inclusion of the spleen in RT ports in all cases; and a short lumbo-aortic port in CS I and II.
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PMID:Hodgkin's disease, clinical stages IA to IIIB: combined modality therapy (3 MOPP followed by curative and prophylactic radiotherapy including the spleen). Six-year results. 369 58

Pathologic flail chest complicated the initial presentation of multiple myeloma in two patients. Both had severe hypercalcemia and diffuse bone disease. Atelectasis and pulmonary edema preceded the appearance of flail chest in one patient; atelectasis complicated the flail chest in the second patient and increased the severity of the flail. Both were treated with radiotherapy and chemotherapy. However, delay in stabilizing the first patient's chest wall with positive airway pressure was followed by extension of the flail chest and irreversible respiratory failure. On the other hand, prolonged stabilization of the chest wall in the second patient until a chemotherapy-induced remission occurred was associated with resolution of the flail chest.
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PMID:Pathologic flail chest complicating multiple myeloma. 736 61

A high cardiac output state, with or without congestive heart failure, has recently been recognized in patients with multiple myeloma. This case report deals with a 62-year-old man with multiple myeloma refractory to treatment, a high cardiac output state, and life-threatening pulmonary edema. In addition, a brief review of the literature is presented.
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PMID:High cardiac output state in patients with multiple myeloma: case report and review of the literature. 786 42

High cardiac output failure/state (HCOF) is regular feature of some illnesses e.g. thiamine deficiency, hyperthyroidism, severe anemia, Paget's disease or arteriovenous fistulae. HCOF in multiple myeloma is reported quite rarely. 31-year-old man was admitted because of fatigue, dyspnea and subfebrilities. Heart rate was 116/min, sinus rythm blood pressure 110/60 mmHg. Chest film showed cardiomegaly with sings of interstitial pulmonary edema, echocardiography mild dilatation of the left ventricle with hyperkinetic wall motion and small pericardial effusion. Hemoglobin was 104 g/l, leukocyte count 13.5 x 10(9)/l with 30% of plasmatic cells. Serum protein electrophoresis demonstrated a monoclonal gammapathy, X ray studies of the skelet multiple osteolytic lesions. Diagnosis of plasmocytic leukemia-form of multiple myeloma was established and chemotherapy (vincristine + adriamycine + dexamethason) was started. Patient cardiac status deteriorated. Cardiac catheterisation demonstrated mean righ atrial pressure of 25 mmHg, mean pulmonary artery pressure of 28 mmHg and pulmonary artery wedge pressure of 24 mmHg. Co was 20.0 l/min (C.I. 11.5 l/min/m2). In continuing of chemotherapy and symptomatic therapy for heart failure patients status gradually improved and complete remission of the myeloma and normalisation of cardiac parameters was achieved. Heart failure in multiple myeloma patients has been attributed to amyloidosis of myocardium, hyperviscosity syndrome, co-existing CAD or anthracycline toxicity. HCOF should be considered in patients with clinical evidence of heart failure and normal left ventricular function.
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PMID:[Hypercirculatory heart failure in a patient with plasmacytic leukemia]. 855 97

Mesenteric panniculitis is a rare disease of the bowel mesentery, characterized by tumor-like infiltration by chronic inflammatory cells, fat necrosis, and fibrosis. Reported cases cited clinical presentation ranging from abdominal pain to fever of unknown origin, the majority of which were idiopathic and associated with a benign prognosis. We report the case of a 43-yr-old male who presented with malaise, weight loss, microcytic anemia, and a high erythrocyte sedimentation rate. Radiographic and histological investigations revealed typical features of mesenteric panniculitis. Initial treatment with high-dose oral prednisolone led to rapid and complete resolution of symptomatology, radiographic, and laboratory anomalies. Within 6 months, the patient presented again with anemia, renal failure, and hypercalcemia. A diagnosis of IgA kappa chain myeloma was made. Despite chemotherapy and restoration of normocalcemia, he died from refractory pulmonary edema. This is the first report of a hematological malignancy initially presenting with features of mesenteric panniculitis culminating in an aggressive course and a fatal outcome.
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PMID:Aggressive multiple myeloma presenting as mesenteric panniculitis. 1119 60

Thalidomide is an effective therapy for multiple myeloma, although its mechanisms of action remain unclear. Light chain-associated (AL) amyloidosis is a plasma cell disorder related to multiple myeloma, but in AL amyloidosis, fibrillar tissue deposits of clonal immunoglobulin light chains produce organ dysfunction. To test the toxicity and efficacy of thalidomide in AL amyloidosis we initiated a phase I/II trial for patients with AL amyloidosis, most of whom had failed prior therapy with high-dose melphalan and autologous stem cell transplantation. This trial was designed as an individualized 6-month dose-escalation study with reevaluation of bone marrow plasmacytosis and serum and urine monoclonal proteins after 3 and 6 months. Sixteen patients were enrolled in the study with a median age of 62 years (range, 37-70 years). Fourteen patients had renal involvement, 4 had cardiac involvement, 4 had liver involvement, and 2 had predominant soft tissue or lymph node involvement. The median maximum tolerated dose was 300 mg, with fatigue and other central nervous system side effects being the major dose-limiting toxicities. Side effects not frequently reported for other patient populations included exacerbation of peripheral and pulmonary edema and worsening azotemia. In all, 50% of patients experienced grade 3/4 toxicity, and 25% had to discontinue the study drug. No complete hematologic responses were seen, but 25% of patients had a significant reduction in Bence-Jones proteinuria. Thus, while thalidomide has activity in AL amyloidosis, it also has significant toxicity in this patient population.
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PMID:Tolerability and efficacy of thalidomide for the treatment of patients with light chain-associated (AL) amyloidosis. 1267 75

Incidence of malignancies in patients on dialysis is higher than in the comparable population. The topic is discussed from different points of view: A. Malignancy as a cause of renal failure (renal and urinary tract tumors, von Hippel-Lindau disease, Wilms tumor, multiple myeloma, tumors that compress urinary tract). B. Treatment of malignancies may result in renal failure and dialysis (nephrectomy, tumor-lysis syndrome, postradiation fibrosis, direct toxic effect of chemotherapy). C. Dialyzed patients are in higher risk of malignancies, especially those of the kidney and urinary tract but also of pharynx and larynx, thyroid gland etc. The following factors may play some roles: the basic disease, (e.g. analgesic and Balcan nephropathies, China Herba nephropathy etc.), changed metabolic milieu with retention of carcinogens, deficiency of selenium and other substances, acquired renal cysts, compromised immunity, decreased "wash-effect" in oligo-anuria and possible influence of dialysis itself (contact with phtalates, ethylenoxide, nitrosamines etc.). D. Special problems in diagnostics of malignancies. Controversial validity of s.c. "tumor markers" is mentioned. Among the causes of death in dialyzed patients cardiovascular and infectious diseases predominate. The active search for renal and urinary tract tumors should be performed. All other diagnostic procedures depend on the individual patient's risk profile. E. Methods of renal substitution are used in the treatment of malignancies (e.g. dialysis in the tumor-lysis syndrome, plasma filtration to remove paraproteins, intraperitoneal administration of chemotherapy similar to peritoneal dialysis approach). F. Malignant tumors and dialysis--some ethical problems. Withdrawal of dialysis in severely suffering patients should be approved by an informed patient and followed by maximal palliative therapy including palliative ultrafiltration if threat of lung edema occurs.
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PMID:[Malignancies in patients on dialysis]. 1601 14

Hypercalcemia is a common paraneoplastic syndrome that may result in metastatic calcification. We report here on four autopsy cases with paraneoplastic hypercalcemia with metastatic calcification, to evaluate the clinicopathologic manifestations. All were males, aged 37-63 years old. Primary tumors included one transitional cell carcinoma of the urinary bladder, one multiple myeloma, and two squamous cell carcinomas of the esophagus. Calcium concentrations ranged from 3.3 to 5.9 mmol/L. Chronic hypercalcemia resulted in metastatic calcification. The kidney and stomach were the most vulnerable organs. Only case 1 presented with an increase in plasma calcium above 5 mmol/L (about twice the normal value); the metastatic calcification involved the capillary walls of his lungs, and he died of fulminant pulmonary edema. Our conclusion is that judicious treatment for paraneoplastic hypercalcemia is important with respect to the occurrence of pulmonary edema associated with metastatic calcification.
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PMID:Paraneoplastic hypercalcemia with metastatic calcification--clinicopathologic studies. 1656 25


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